Myocardial fibers in the heart wall form a remarkable mechanical system, designed to amplify small amounts of sarcomere shortening into vigorous thickening, and then to recoil briskly, allowing sudden, rapid filling. This project is designed to continue our project relating local deformation to global parameters of function, using two unique methodologies. MRI tissue tagging is a powerful new imaging technique, developed in our laboratory and now widely used, which permits the non- invasive tracking of tissue through the cardiac cycle and accurate measurement of local deformation over the entire LV. The isolated, blood perfused canine heart model is a preparation that we have adapted to the magnetic environment, that allows precise computer driven servo-pump control of preload, afterload, and cavity volume. In our previous work, we demonstrated the importance of the interaction among layers of the heart wall for systolic deformation. We now expand our investigations to diastole. As the ventricle ejects, it exhibits a wringing motion, termed "torsion". We and others have evidence suggested hat potential energy may be stored during this torsional deformation, and that the rapid diastolic recoil of LV torsion, which occurs largely during isovolumic relaxation when cavity volume is fixed, may create suction to aid early diastolic filling. We now aim to correlate the speed and timing of this recoil with the effectiveness of early diastolic filling in a group of patients known to have filling abnormalities: hypertensives. We will also study hypertension since the isolated heart model allows the measurement of global diastolic suction. We will clarify the role of the interstitial connective tissue matrix in the heart in the coordination of deformation in systole, and the development of suction in diastole, using a model of connective tissue dysfunction (lathyrism). In other studies we will characterize the load dependence of torsion, and the effects of altered septal geometry on deformation. The results will have important implications in processes characterized by reduced early diastolic filling, which we suspect is related to abnormal recoil of systolic deformations. These processes include hypertension, congestive heart failure, and also aging itself. They should clarify aspects of wall deformation in myocardial diseases characterized by abnormal collagen including cardiomyopathy, myocardial infarction, expansion, and stunning. They will add to the understanding of LV dysfunction in disease processes that alter ventricular geometry, such as right ventricular overload states.